Hyponatremia and Increased Exchangeable Sodium in Chronic Obstructive Lung Disease

Bauer, Franz K.; Telfer, Nancy; Herbst, Harry H.; Austin, Robert; Hetter, Brita

doi:10.1097/00000441-196509000-00001

Cited by 21 publications

(17 citation statements)

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“…All the data are summarized in Table1 and 2. [10][11][12] This is in agreement with the study by Das et al, who measured the serum K+ and Na+ in 64 patients with acute exacerbation of COPD and compared the results with 20 healthy volunteers. 12 They reported a significant decrease in serum Na+ and K+ in COPD patients (133±6.86 mEq/lit, 3.39±0.96 mEq/lit respectively) than in normal controls (142±2.28 mEq/lit, 4.52±0.02 mEq/lit respectively, p<0.05).…”

Section: Resultssupporting

confidence: 88%

Study of serum electrolytes in acute exacerbation of chronic obstructive pulmonary disease patients

Goli¹,

Mukka²,

Sairi³

2016

Int J Res Med Sci

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Section: Resultssupporting

confidence: 88%

Study of serum electrolytes in acute exacerbation of chronic obstructive pulmonary disease patients

Goli¹,

Mukka²,

Sairi³

2016

Int J Res Med Sci

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“…The mean of the 2nd group is significantly (p < 0.02) less than that of the controls. This finding was already pointed out by other authors [Bauer et al, 1965], as well as by ourselves [Sadoul et al, 1967]. It is perhaps a question of hyponatremia by dilution, or a A (c -a ) Pco 2 -i mm Hg *10- displacement toward the interstitial fluids, or another mechanism.…”

Section: Electrolyte Balancesupporting

confidence: 62%

Acid Base and Electrolyte Equilibrium of Arterial Blood and Cerebro-spinal Fluid in Respiratory Insufficiency

Saunier¹,

Aug-Laxenaire²,

Schibi³

et al. 1969

Respiration

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“…This would mean that oedema formation is not, or at least not always, simply due to accumulation but rather to redistribution of fluid. On the other hand, there is data to show that the ECV is expanded in COPD [9][10][11]. One such example is the study of ANAND et al [11].…”

Section: Body Fluid Volumes In Chronic Obstructive Pulmonary Diseasementioning

confidence: 99%

Fluid homeostasis in chronic obstructive lung disease

Leeuw¹,

Dees²

2003

Eur Respir J

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Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases.Cardiac output is remarkably normal, suggesting that “cor pulmonale” is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodiumretaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapniainduced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles rightsided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.

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Hyponatremia and Increased Exchangeable Sodium in Chronic Obstructive Lung Disease

Cited by 21 publications

References 0 publications

Study of serum electrolytes in acute exacerbation of chronic obstructive pulmonary disease patients

Study of serum electrolytes in acute exacerbation of chronic obstructive pulmonary disease patients

Acid Base and Electrolyte Equilibrium of Arterial Blood and Cerebro-spinal Fluid in Respiratory Insufficiency

Fluid homeostasis in chronic obstructive lung disease

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